Cocooned within the bowels of the Earth, one mineral’s metamorphosis into another may trigger some of the deepest earthquakes ever detected.
These cryptic tremors — known as deep-focus earthquakes — are a seismic conundrum. They violently rupture at depths greater than 300 kilometers, where intense temperatures and pressures are thought to force rocks to flow smoothly. Now, experiments suggest that those same hellish conditions might also sometimes transform olivine — the primary mineral in Earth’s mantle — into the mineral wadsleyite. This mineral switch-up can destabilize the surrounding rock, enabling earthquakes at otherwise impossible depths, mineral physicist Tomohiro Ohuchi and colleagues report September 15 in Nature Communications. “It’s been a real puzzle for many scientists because earthquakes shouldn’t occur deeper than 300 kilometers,” says Ohuchi, of Ehime University in Matsuyama, Japan.
Deep-focus earthquakes usually occur at subduction zones where tectonic plates made of oceanic crust — rich in olivine — plunge toward the mantle (SN: 1/13/21). Since the quakes’ seismic waves lose strength during their long ascent to the surface, they aren’t typically dangerous. But that doesn’t mean the quakes aren’t sometimes powerful. In 2013, a magnitude 8.3 deep-focus quake struck around 609 kilometers below the Sea of Okhotsk, just off Russia’s eastern coast.
Past studies hinted that unstable olivine crystals could spawn deep quakes. But those studies tested other minerals that were similar in composition to olivine but deform at lower pressures, Ohuchi says, or the experiments didn’t strain samples enough to form faults.
He and his team decided to put olivine itself to the test. To replicate conditions deep underground, the researchers heated and squeezed olivine crystals up to nearly 1100° Celsius and 17 gigapascals. Then the team used a mechanical press to further compress the olivine slowly and monitored the deformation.
From 11 to 17 gigapascals and about 800° to 900° C, the olivine recrystallized into thin layers containing new wadsleyite and smaller olivine grains. The researchers also found tiny faults and recorded bursts of sound waves — indicative of miniature earthquakes. Along subducting tectonic plates, many of these thin layers grow and link to form weak regions in the rock, upon which faults and earthquakes can initiate, the researchers suggest.
“The transformation really wreaks havoc with the [rock’s] mechanical stability,” says geophysicist Pamela Burnley of the University of Nevada, Las Vegas, who was not involved in the research. The findings help confirm that olivine transformations are enabling deep-focus earthquakes, she says.
Next, Ohuchi’s team plans to experiment on olivine at even higher pressures to gain insights into the mineral’s deformation at greater depths.
Art historian Erin Griffey is a bit of a beauty maven. “I’m one of those people who reads the backs of beauty products,” she says. That’s why, while working on a book about beauty culture in Renaissance Europe, Griffey experienced déjà vu.
She noticed that many ingredients in beauty recipes from the 16th to 18th centuries — compiled from books, cosmetic recipe collections, medical texts, health regimen manuscripts, herbals and pharmacopeias — also appear on modern beauty packaging. For instance, rosewater is used in modern skin-hydrating mists and sulfur is found in some over-the-counter acne creams. Such similarities are clues to what Renaissance-era people used the products for and how the products worked. But they are not the whole story. That’s because the ancient recipes often also list bizarre or even dangerous ingredients, from bile acids and calves’ hooves to lead and the poisonous bryony plant. To get a better understanding, Griffey wanted to re-create the recipes. So she turned to her colleagues at the University of Auckland in New Zealand. Thus the Beautiful Chemistry Project was born.
The team started with what Griffey calls “sticky recipes” because they’re found in many sources throughout the Renaissance period: rosemary flowers in white wine, myrrh powder with egg white, and the velvety covering of newly grown deer antlers with bean flour.
The recipes tend to be vague and varied. So chemist Michel Nieuwoudt and her team experiment with the measurements and procedures while Griffey searches various sources for more clues to ingredient types and ratios.
“We knew we could not re-create it exactly as is,” Griffey says of the recipe for rosemary flowers in white wine. “We do not have access to the rosemary plants that grew 500 years ago or the wines and whatever their chemical makeup was.” But this legwork “enabled us to get closer to an approximation.”
Nieuwoudt and her team boiled rosemary flowers in round-bottom flasks each filled with a different solution: sweet white wine, dry white wine, ethanol in water or aqua vitae. Once the researchers filtered out the flowers and analyzed the resulting mixtures using gas chromatography and mass spectrometry, they found chemical compounds that are common in today’s skin care products, including soothing camphor, eucalyptol and the fragrant alcohol linalool (SN: 7/22/02).
The Renaissance-era recipe stated the potion would “make the face fair.” Nieuwoudt’s findings suggest how: by toning and moisturizing skin. The team has also made progress on unlocking the secrets of myrrh powder and egg whites. Experiments suggest that myrrh draws out proteins from egg whites and the egg whites extract resins, sugars and volatiles from the myrrh. That results in a serumlike product that has antiseptic and anti-inflammatory properties and probably stimulates collagen growth, Nieuwoudt says. “It seems there’s a synergy between all of these different ingredients, and this is why it works.”
As for what deer velvet and bean flour may have been used for, the researchers are still teasing out results. And they have yet to tackle recipes with dangerous ingredients.
Eventually, the researchers hope to perfect their re-creations and bring the products to drug store shelves — minus, of course, any unsafe ingredients. “I think people will want to go back to something that is natural, and it’s also appealing for people to think they’re using Renaissance products,” Nieuwoudt says. Until then, the beauty for the researchers lies in “digging [the recipes] out and understanding them.”
If whole organs could be frozen and stored … surgeons would be able to perform far more transplants…. For all their efforts, though, cryobiologists (biologists who study the effects of cold on life) have not been very successful with organ freezing…. Nobody to date has cooled whole mammalian hearts any lower [than −20° Celsius] or longer [than six hours] and revived them.
Update Scientists still struggle to keep donor hearts on ice for longer than six hours, but it is now possible to store a different organ — the liver — at below-freezing temperatures for more than a day. The challenge has been figuring out how to stop ice from crystallizing and damaging cells. In 2019, scientists reported successfully warming up several human livers after supercooling them for 27 hours (SN: 10/12/19 & 10/26/19, p. 10). This and other preservation methods such as freezing at high pressures or thawing using nanoparticles aren’t yet ready for the operating room, but they have the potential to keep thousands of lifesaving organs from going to waste each year.
For some people, including President Joe Biden and National Institute of Allergy and Infectious Diseases director Anthony Fauci, the relief of vanishing COVID-19 symptoms and a negative test is fleeting. Biden, Fauci and many others have seen their tests turn positive again or have unwelcome symptoms return after taking a five-day course of the antiviral Paxlovid. Other people, including my husband, have had their infections rebound even without taking the drug.
Multiple studies have described cases of “Paxlovid rebound” after treatment. In one, seven Paxlovid-treated patients had the virus rebound to high levels after treatment ended, and symptoms returned for six of them, virologist Jonathan Li and colleagues reported in June in Clinical Infectious Diseases. Samples from three patients even carried infectious virus, a clue that some people who rebound might infect others. Another study that has yet to be peer-reviewed by other researchers found that fewer than 6 percent of people in the study who’d been prescribed Paxlovid had rebound infections in the month after finishing treatment. It’s unclear why Paxlovid rebound happens, says Li, of Brigham and Women’s Hospital and Harvard Medical School. Studies show that people given the drug still develop a strong immune response to the virus after five days of treatment. “I think what’s happening in that situation is that you’ve got virus replication that’s been inhibited. All of a sudden, the drug has disappeared and the virus has a momentary opportunity to replicate. And it replicates to high levels,” Li says. But by then, the immune system has learned to fend off the coronavirus. If the recently trained immune cells encounter newly made viruses and set off alarm bells, symptoms may briefly come back.
Some people might not want to take the drug because they’re worried about rebound, Li says. But Paxlovid itself probably isn’t the cause. The drug’s not failing. It is still highly effective in preventing severe disease. “I would not hesitate to give my patients Paxlovid,” Li says. “I do tell them to be on the lookout for rebounding symptoms. But it doesn’t dissuade me in terms of prescribing it.”
Fauci took another course of Paxlovid in the wake of his rebound. The U.S. Food and Drug Administration says that there’s no evidence that 10 days of treatment is any more effective than five days, or that patients need a repeat. But, researchers are testing whether taking the drug for a longer period of time might prevent rebound.
Rebounding COVID-19 isn’t limited to patients who take Paxlovid. Li recalls that even in the early days of the pandemic, some patients would come to him in the hospital saying that they’d started to feel better but got worse again. It’s hard to know how to interpret such anecdotal reports, he says. Researchers are still learning what an untreated viral infection can look like in the body. While the virus’s (hopefully) brief invasion may appear straightforward on average — with virus levels in the body increasing to a peak before slowly declining as the person recovers — not everyone follows that pattern. My husband got COVID-19 two months ago. His symptoms lasted about a week, and he was delighted to see the line on his antigen test getting fainter. Even so, despite feeling perfectly healthy, the line was suddenly back at full strength almost immediately after he added his sample to a new test days later. He was frustrated and, as a social person, lamented having to stay isolated.
Studies show he’s not alone. When Li and colleagues studied the course of disease in COVID-19 clinical trial participants who received a placebo treatment, 1 in 8 people experienced a rebound, with symptoms coming back for 1 in 4 people. That rebound, however, typically lasted about a day, and few had both high viral loads and returning symptoms, the team reports in a preliminary study posted August 2 at medRxiv.org that hasn’t yet been peer-reviewed by other scientists.
In this case, there’s no disappearing drug. Any returning symptoms without a positive test might be from something else such as allergies or a different respiratory virus, Li says. It’s also possible that the virus is replicating in different parts of the body at different times. Some tests might end up negative when the body eliminates virus from the throat, for example, but it’s still replicating at low levels in the nose.
That latter scenario may have happened with my husband. In a confusing twist, he tested negative on two saliva PCR tests while continuing to test positive on nasal antigen tests. A PCR test is far more sensitive, so we expected the opposite to happen. Since experts say to consider a positive antigen test as a sign you’re still contagious, he stayed isolated until he finally tested negative on an antigen test two weeks after his first symptoms appeared.
Luckily, he’s fully recovered now, and not at all eager for a repeat experience. That means we’re both still masking in public spaces and taking other precautions. We know we’re not done with this pandemic.
It may soon be too late to end the global monkeypox epidemic.
“We are losing the window to be able to contain this outbreak,” Boghuma Titanji, an infectious diseases doctor and virologist at Emory University in Atlanta said July 21 during a seminar sponsored by the Harvard Kennedy School’s Belfer Center for Science and International Affairs.
On July 23, Tedros Adhanom Ghebreyesus, director of the World Health Organization declared the global outbreak of monkeypox is a public health emergency of international concern, the organization’s highest state of alert. The WHO committee evaluating the matter was split on whether the outbreak constitutes an international emergency, but Ghebreyesus decided that enough conditions were met to warrant the designation. Monkeypox has infected more than 15,700 people since the beginning of May, according to Global.health (SN: 5/26/22). More than 2,800 cases have been reported in the United States as of July 22, the U.S. Centers for Disease Control and Prevention report.
“Although I am declaring a public health emergency of international concern, for the moment this is an outbreak that is concentrated among men who have sex with men, especially those with multiple sexual partners,” Ghebreyesus said in a statement. “That means that this is an outbreak that can be stopped with the right strategies in the right groups.”
Monkeypox has caused outbreaks for decades in some parts of Africa, Anne Rimoin, an epidemiologist at the UCLA Fielding School of Public Health, said at the Harvard seminar. But the virus “has been neglected by the global health community.” Monkeypox “has been giving us warning signals” for years in Congo, Nigeria and other parts of West Africa, but has only gotten attention once it recently started causing cases outside of the continent, Rimoin said.
There has been no concerted global effort to contain the virus, which is related to smallpox, Titanji said. Each country has been left to set its own policies.
That has led to disparities. Well-resourced countries have had at least some access to testing, vaccines and medications, which may help limit the spread of the virus or the severity of the disease. Resource-poor nations often lack that access, leaving them with limited ability to track or control the virus. Continued spread of monkeypox in resource-poor countries could leave places that do manage to contain an initial outbreak vulnerable to reintroductions, Jay K. Varma, director of the Cornell Center for Pandemic Prevention and Response in New York City, said in the seminar. The WHO emergency declaration may lead to a more concerted international effort that could make more resources available to contain the spread of the virus.
Even for the wealthiest countries, containing the outbreak is a challenge. Questions abound about how the virus is transmitted, and whether vaccines and treatments — when people can get them — can halt its spread. Even diagnosing the disease can be tricky, with testing often hard to come by and missed diagnoses potentially leading to more cases.
The vast majority of monkeypox cases in the global outbreak have been among men who have sex with men. Of 528 people infected with monkeypox in 16 countries, 98 percent identified as gay or bisexual men, researchers report July 21 in the New England Journal of Medicine.
In some countries with outbreaks, “gay men are criminalized,” Kai Kupferschmidt, a correspondent for Science magazine, said during the seminar. In those countries, “people cannot access good information to help them keep from getting infected and cannot access health care if they do get infected. In these countries, it becomes really difficult to even see the problem,” he said.
Ghebreyesus urged all countries to “work closely with communities of men who have sex with men, to design and deliver effective information and services, and to adopt measures that protect the health, human rights and dignity of affected communities. Stigma and discrimination can be as dangerous as any virus,” he said in a statement.
Doctors might also miss cases of monkeypox because of the unusual presentation of the illness in this outbreak, compared with earlier outbreaks. For instance, in the NEJM study, only a quarter of patients had monkeypox lesions on their faces and only 10 percent had the sores on their palms or soles of their feet. Those body parts have been among some of the most affected in other outbreaks.
Instead, 73 percent of people in the study had lesions in the anal and genital regions and 55 percent on the trunk, arms or legs. Some people also had lesions in their mouths and throats. Most of the people in the study had fewer than 10 lesions, with 54 people having only a single lesion on their genitals, making confusion with herpes or syphilis possible, even easy.
Seventy people in the study were admitted to the hospital. Of those, 21 were hospitalized because of pain, mostly severe rectal pain. Others had eye lesions, kidney damage, inflammation of the heart or throat swelling that prevented them from taking in liquids.
Those complications fit with what health officials across the United States have been seeing. “While mortality appears very low, which is great, morbidity has been much higher than any of us expected,” Mary Foote, the medical director of the New York City Department of Health and Mental Hygiene, said July 14 in a news briefing sponsored by the Infectious Diseases Society of America.
“A lot of people with this infection are really suffering, and some may be at risk of permanent damage and scarring. We see many people with symptoms so severe that they are unable to go to the bathroom, urinate or eat without excruciating pain,” Foote said.
A small number of women and children have also gotten monkeypox in the outbreak. Two children in the United States have been diagnosed with monkeypox, CDC director Rochelle Walensky said July 22 in an interview with the Washington Post. Both children were social contacts of men that have sex with men, she said.
A child in the Netherlands who had no contact with anyone known to be infected with the virus also got monkeypox, researchers report July 21 in Eurosurveillance. His case raises the possibility that monkeypox may be spreading undetected more broadly in communities than realized.
“I don’t think it’s surprising that we are occasionally going to see cases in individuals who are not gay, bisexual or other men who have sex with men. The social networks we have as humans mean we have contact with a lot of different people,” Jennifer McQuiston, deputy director of the CDC’s Division of High Consequence Pathogens and Pathology said July 22 during a White House news briefing.
Exactly how the child in the Netherlands became infected is a matter of speculation. Monkeypox typically spreads among people through close contact with infected people or with clothing, bedding or towels used by people with the disease. Examination of viral DNA showed that the boy isn’t connected to any of the known cases in the Netherlands. He traveled to Turkey in June and may have gotten infected there or while traveling.
The boy has very low levels of IgA antibodies, which patrol mucous membranes and help prevent infections there. Low levels of the antibodies could make him vulnerable to respiratory infections. People can get infected with monkeypox through droplets given off by infected people during close face-to-face interactions, such as close conversation, kissing or during medical exams. But patterns of infection clearly indicate that monkeypox isn’t airborne the way COVID-19 or other respiratory viruses are, Kupferschmidt said.
Details of how monkeypox spreads are still unknown. For instance, researchers don’t know whether the virus can be transmitted through semen as a sexually transmitted disease. Researchers have found evidence of viral DNA in semen, saliva, urine and feces, but that may just be inactive remnants of the virus. So far, no researchers have reported finding infectious virus in genital body fluids that might be exchanged during sex. Also unknown is whether getting infected through mucous membranes during sexual contact would shield against catching the virus later, Rimoin said.
Scientists are questioning whether the monkeypox virus has changed or whether it has simply found a niche social-sexual network among gay and bisexual men that may enable the virus to spread more efficiently, Titanji said. It may be that there are different transmission patterns in historically affected countries and newly affected countries that require different strategies to stop the spread, she said.
Researchers also need to do good studies to figure out how well vaccines and therapeutics work and under what circumstances, Rimoin said. WHO’s emergency declaration includes recommendations for increasing testing and surveillance and for seeding up research on vaccines, treatments and other virus containment measures.
One thing is clear, Rimoin said. “We’re giving this virus room to run like it never has before.” People have passed the buck, leaving others to work out the problem of monkeypox, she said. But now, “it’s everybody’s problem to solve.”
Sci-fi novels and films like Gattaca no longer have a monopoly on genetically engineered humans. Real research scripts about editing the human genome are now appearing in scientific and medical journals. But the reviews are mixed.
In Gattaca, nearly everyone was genetically altered, their DNA adjusted to prevent disease, enhance intelligence and make them look good. Today, only people treated with gene therapy have genetically engineered DNA. But powerful new gene editing tools could expand the scope of DNA alteration, forever changing humans’ genetic destiny.
Not everyone thinks scientists should wield that power. Kindling the debate is a report by scientists from Sun Yat-sen University in Guangzhou, China, who have edited a gene in fertilized human eggs, called zygotes. The team used new gene editing technology known as the CRISPR/Cas9 system. That technology can precisely snip out a disease-causing mutation and replace it with healthy DNA. CRISPR/Cas9 has edited DNA in stem cells and cancer cells in humans. Researchers have also deployed the molecules to engineer other animals, including mice and monkeys (SN Online: 3/31/14; SN: 3/8/14, p. 7). But it had never before been used to alter human embryos. The team’s results, reported April 18 in Protein & Cell, sparked a flurry of headlines because their experiment modified human germline tissue (SN Online: 4/23/15). While most people think it is all right to fix faulty genes in mature body, or somatic, cells, tinkering with the germ line — eggs, sperm or tissues that produce those reproductive cells — crosses an ethical line for many. Germline changes can be passed on to future generations, and critics worry that allowing genetic engineering to correct diseases in germline tissues could pave the way for creating designer babies or other abuses that will persist forever.
“How do you draw a clear, meaningful line between therapy and enhancement?” ponders Marcy Darnovsky, executive director of the Center for Genetics and Society in Berkeley, Calif. About 40 countries ban or restrict such inherited DNA modifications.
Rumors about human germline editing experiments prompted scientists to gather in January in Napa, Calif. Discussions there led two groups to publish recommendations. One group, reporting March 26 in Nature, called for scientists to “agree not to modify the DNA of human reproductive cells,” including the nonviable zygotes used in the Chinese study. A second group, writing in Science April 3, called for a moratorium on the clinical use of human germline engineering, but stopped short of saying the technology shouldn’t be used in research. Those researchers say that while CRISPR technology is still too primitive for safe use in patients, further research is needed to improve it. But those publishing in Nature disagreed.
“Are there ever any therapeutic uses that would demand … modification of the human germ line? We don’t think there are any,” says Edward Lanphier, president of Sangamo BioSciences in Richmond, Calif. “Modifying the germ line is crossing the line that most countries on our planet have said is never appropriate to cross.”
If germline editing is never going to be allowed, there is no reason to conduct research using human embryos or reproductive cells, he says. Sangamo BioSciences is developing gene editing tools for use in somatic cells, an approach that germline editing might render unneeded. Lanphier denies that financial interests play a role in his objection to germline editing.
Other researchers, including Harvard University geneticist George Church, think germline editing may well be the only solution for some people with rare, inherited diseases. “What people want is safety and efficacy,” says Church. “If you ban experiments aimed at improving safety and efficacy, we’ll never get there.”
The zygote experiments certainly demonstrate that CRISPR technology is not ready for daily use yet. The researchers attempted to edit the beta globin, or HBB, gene. Mutations in that gene cause the inherited blood disorder beta-thalassemia. CRISPR/Cas9 molecules were engineered to seek out HBB and cut it where a piece of single-stranded DNA could heal the breach, creating a copy of the gene without mutations. That strategy succeeded in only four of the 86 embryos that the researchers attempted to edit. Those edited embryos contained a mix of cells, some with the gene edited and some without.
In an additional seven embryos, the HBB gene cut was repaired using the nearby HBD gene instead of the single-stranded DNA. The researchers also found that the molecular scissors snipped other genes that the researchers never intended to touch.
“Taken together, our work highlights the pressing need to further improve the fidelity and specificity of the CRISPR/Cas9 platform, a prerequisite for any clinical applications,” the researchers wrote.
The Chinese researchers crossed no ethical lines, Church contends. “They tried to dot i’s and cross t’s on the ethical questions.” The zygotes could not develop into a person, for instance: They had three sets of chromosomes, having been fertilized by two sperm in lab dishes.
Viable or not, germline cells should be off limits, says Darnovsky. She opposes all types of human germline modification, including a procedure approved in the United Kingdom in February for preventing mitochondrial diseases. The U.K. prohibits all other germline editing.
Mitochondria, the power plants that churn out energy in a cell, each carry a circle of DNA containing genes necessary for the organelle’s function. Mothers pass mitochondria on to their offspring through the egg. About one in 5,000 babies worldwide are born with mitochondrial DNA mutations that cause disease, particularly in energy-greedy organs such as the muscles, heart and brain.
Such diseases could be circumvented with a germline editing method known as mitochondrial replacement therapy (SN: 11/17/12, p. 5). In a procedure pioneered by scientists at Oregon Health & Science University, researchers first pluck the nucleus, where the bulk of genetic instructions for making a person are stored, out of the egg of a woman who carries mutant mitochondria. That nucleus is then inserted into a donor egg containing healthy mitochondria. The transfer would produce a person with three parents; most of their genes inherited from the mother and father, with mitochondrial DNA from the anonymous donor. The first babies produced through that technology could be born in the U.K. next year.
Yet another new gene-editing technique could eliminate the need to use donor eggs by specifically destroying only disease-carrying mitochondria, researchers from the Salk Institute for Biological Studies in La Jolla, Calif., reported April 23 in Cell (SN Online: 4/23/15).
Such unproven technologies shouldn’t be attempted when alternatives already exist, Darnovsky says, such as screening embryos created through in vitro fertilization and discarding those likely to develop the disease.
But banning genome-altering technology could leave people with genetic diseases, and society in general, in the lurch, says molecular biologist Matthew Porteus of Stanford University.
“There is no benefit in my mind of having a child born with a devastating genetic disease,” he says.
Alternatives to germline editing come with their own ethical quandaries, he says. Gene testing of embryos may require creating a dozen or more embryos before finding one that doesn’t carry the disease. The rest of the embryos would be destroyed. Many people find that prospect ethically questionable.
But that doesn’t argue for sliding into Gattaca territory, where genetic modification becomes mandatory. “If we get there,” says Porteus, “we’ve really screwed up.”
